What is the primary mechanism of goitre formation in a euthyroid (having a normally functioning thyroid gland) woman from an iodine-deficient region who has developed a diffuse goitre?

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Primary Mechanism of Goitre Formation in Iodine Deficiency

The correct answer is C: Chronic TSH stimulation is the primary mechanism of goitre formation in a euthyroid woman from an iodine-deficient region with diffuse goitre.

Pathophysiological Mechanism

In iodine deficiency, the thyroid gland experiences chronic TSH stimulation as a compensatory response to maintain euthyroid status, which directly causes thyroid enlargement (goitre). 1

The mechanism operates through the following sequence:

  • TSH regulates all steps of thyroid hormone biosynthesis, including iodide uptake, oxidation and organification of iodide, and secretion of T4 and T3 into circulation 1, 2

  • When iodine is deficient, the thyroid cannot produce adequate thyroid hormone despite increased TSH-driven activity, leading to compensatory thyroid gland enlargement to maximize iodine uptake and recycling 1

  • The patient remains euthyroid because the increased thyroid activity and gland size compensate for low iodine availability, maintaining normal thyroid hormone production despite the deficiency 1

Why Other Options Are Incorrect

Option A (Autoimmune stimulation) is incorrect because this describes Graves' disease, not iodine-deficiency goitre 3

Option B (Excess thyroid hormone synthesis) is incorrect because the patient is euthyroid, not hyperthyroid, and iodine deficiency actually impairs hormone synthesis 1

Option D (Thyroid hormone resistance) is incorrect because this is a genetic disorder unrelated to iodine deficiency 2

Option E (Increased thyroglobulin destruction) is incorrect because goitrogenesis involves increased thyroid activity and growth, not destruction of thyroglobulin 1

Important Clinical Nuances

TSH levels may remain within normal range despite frank iodine deficiency, making TSH an insensitive indicator of iodine status 1, 4. This explains why the patient can have a goitre while remaining biochemically euthyroid.

The intrathyroidal iodine concentration is low in endemic goitre, but this is a secondary event rather than the primary cause - the fundamental driver is the chronic TSH stimulation attempting to compensate for inadequate iodine substrate 5

While some research suggests intrinsic thyroid factors may contribute to nodular goitre development 6, 5, the initial diffuse goitre formation in iodine-deficient regions is primarily TSH-mediated 1, 3

References

Guideline

Guideline Directed Topic Overview

Dr.Oracle Medical Advisory Board & Editors, 2025

Guideline

Regulation of Thyroid Hormone Production

Praxis Medical Insights: Practical Summaries of Clinical Guidelines, 2025

Research

Endemic goiter and endemic thyroid disorders.

World journal of surgery, 1991

Guideline

Micronutrient Supplementation for Hypothyroidism Management

Praxis Medical Insights: Practical Summaries of Clinical Guidelines, 2026

Research

Nodular goiter and goiter nodules: Where iodine deficiency falls short of explaining the facts.

Experimental and clinical endocrinology & diabetes : official journal, German Society of Endocrinology [and] German Diabetes Association, 2001

Research

Multinodular goitre: 'much more to it than simply iodine deficiency'.

Bailliere's best practice & research. Clinical endocrinology & metabolism, 2000

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This information is intended for healthcare professionals. Any medical decision-making should rely on clinical judgment and independently verified information. The content provided herein does not replace professional discretion and should be considered supplementary to established clinical guidelines. Healthcare providers should verify all information against primary literature and current practice standards before application in patient care. Dr.Oracle assumes no liability for clinical decisions based on this content.

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